Hippocampal CA1/subiculum-prefrontal cortical pathways induce plastic changes of nociceptive responses in cingulate and prelimbic areas.
Hippocampal CA1/subiculum-prefrontal cortical pathways induce plastic changes of nociceptive responses in cingulate and prelimbic areas.
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DOI：
10.1186/1471-2202-11-100
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发表时间：
2010-08-17
期刊：
影响因子：
2.4
通讯作者：
Kawakami Y
中科院分区：
文献类型：
--
作者：
Nakamura H;Katayama Y;Kawakami Y
海马CA 1-下托（CA 1/SB）区向前额叶皮质（PFC）的投射参与记忆和学习过程，使PFC神经元产生长时程突触可塑性。在PFC内记录到机械伤害性刺激引起的细胞外单位放电和单一刺激脉冲引起的场电位，并观察了这些投射对PFC边缘前区和扣带区伤害性反应的调节作用（HFS，100 Hz）传递到CA 1/SB，产生场电位的长时程增强（LTP），在78%的情况下诱导伤害性反应的长时程增强（LTE），而相反地，在22%的情况下反应降低（长时程抑郁，LTD）。这些神经元分散在扣带和边缘前区。场电位和伤害性放电的结果表明，CA 1/SB-PFC途径可以产生异突触增强PFC神经元。HFS对扣带回皮质Fos表达无影响。低频电刺激（LFS，1Hz，600次脉冲）在所有病例中均诱发伤害性放电LTD。从LTD恢复后，向CA 1/SB递送HFS具有相反的作用，在同一神经元中诱导伤害性反应的LTE。双向型的可塑性是明显的，在这些伤害性反应，在homosynaptic可塑性先前报道。诱导LTD的神经元主要位于边缘前区，其中Fos表达也被LFS抑制。电生理结果与免疫染色结果接近。我们的研究结果表明，CA 1/SB-PFC途径抑制兴奋性锥体细胞的活动，在前边缘区。压力刺激（300 g）施加到大鼠的尾巴引起的伤害性反应的扣带和边缘前区的PFC，其中接收直接通路从CA 1/SB。HFS和LFS传递到CA 1/SB引起的伤害性反应的长期可塑性。因此，CA 1/SB-PFC投射调节PFC神经元的伤害性反应。
Projections from hippocampal CA1-subiculum (CA1/SB) areas to the prefrontal cortex (PFC), which are involved in memory and learning processes, produce long term synaptic plasticity in PFC neurons. We examined modifying effects of these projections on nociceptive responses recorded in the prelimbic and cingulate areas of the PFC. Extracellular unit discharges evoked by mechanical noxious stimulation delivered to the rat-tail and field potentials evoked by a single stimulus pulse delivered to CA1/SB were recorded in the PFC. High frequency stimulation (HFS, 100 Hz) delivered to CA1/SB, which produced long-term potentiation (LTP) of field potentials, induced long-term enhancement (LTE) of nociceptive responses in 78% of cases, while, conversely, in 22% responses decreased (long-term depression, LTD). These neurons were scattered throughout the cingulate and prelimbic areas. The results obtained for field potentials and nociceptive discharges suggest that CA1/SB-PFC pathways can produce heterosynaptic potentiation in PFC neurons. HFS had no effects on Fos expression in the cingulated cortex. Low frequency stimulation (LFS, 1 Hz, 600 bursts) delivered to the CA1/SB induced LTD of nociceptive discharges in all cases. After recovery from LTD, HFS delivered to CA1/SB had the opposite effect, inducing LTE of nociceptive responses in the same neuron. The bidirectional type of plasticity was evident in these nociceptive responses, as in the homosynaptic plasticity reported previously. Neurons inducing LTD are found mainly in the prelimbic area, in which Fos expression was also shown to be inhibited by LFS. The electrophysiological results closely paralleled those of immunostaining. Our results indicate that CA1/SB-PFC pathways inhibit excitatory pyramidal cell activities in prelimbic areas. Pressure stimulation (300 g) applied to the rat-tail induced nociceptive responses in the cingulate and prelimbic areas of the PFC, which receives direct pathways from CA1/SB. HFS and LFS delivered to the CA1/SB induced long-term plasticity of nociceptive responses. Thus, CA1/SB-PFC projections modulate the nociceptive responses of PFC neurons.